A Prospective Look at the Link Between Frailty and Shoulder Function in Asymptomatic Elderly Individuals.

INTRODUCTION: The relationship between shoulder function and overall function in the elderly patients is not well understood. It is hypothesized that there is an increased tolerance of shoulder dysfunction in this population. The purpose of our study was to investigate and better understand the relationship between shoulder function, general musculoskeletal health, and frailty in the elderly patients. MATERIALS AND METHODS: The dominant shoulders of 75 individuals aged ≥65 years without known dominant shoulder pathology were assessed. Demographic data were collected. Functional evaluation was conducted by administering the Constant, American Shoulder and Elbow Surgeons (ASES), and the Short Musculoskeletal Function Assessment (SMFA) questionnaires. Shoulder range of motion and strength were measured and the Fried frailty phenotype was calculated. Mean age of the patients was 73.6 years. Sixty-seven percent of the patients were female. Mean body mass index was 31.2 kg/m2. RESULTS: Twenty-eight percent of the patients reported the use of an assistive device for ambulation. As frailty increased among the 3 Fried frailty phenotypes (robust, prefrail, and frail), patients had statistically significant lower mean Constant scores (P < .0001), ASES scores (P < .0001), higher overall SMFA scores (P < .0001), and an increase in the use of assistive device for ambulation. Individuals who reported the use of an assistive device for ambulation had lower Constant and ASES scores (P < .0001 and P = .045, respectively) and higher overall SMFA scores (P < .0001). There was no evidence of correlation between body mass index and any of the other measures. CONCLUSIONS: Frailty and the use of an assistive device for ambulation correlate with poor shoulder function in patients who do not register shoulder complaints and have no known shoulder pathology. LEVEL OF EVIDENCE: Level IV, Prognostic.

On orthopedic surgical skill prediction--the limited value of traditional testing.

OBJECTIVES: Primary: to assess the utility of our distal radius fracture repair model as a tool for examining residents' surgical skills. Secondary: to compare the residents' ability to achieve specific biomechanically measured fracture stability with traditional test scores. DESIGN: Our laboratory pioneered a model that measures biomechanical qualities of a repaired distal radius fracture. Before participation, all residents to be tested completed specified knowledge examinations. During the laboratory exercise, proctors observed each resident and completed Objective Structured Assessment of Technical Skills forms. At the completion of the laboratory, each specimen was tested biomechanically. Written examinations were completed in a proctored setting and computer examinations at home following the honor system. The laboratory exercise had adequate space and materials and allowed 60 minutes to complete the procedure. Residents had equal access to x-ray imaging. SETTING: The examination environment of the study resembled an operating room. PARTICIPANTS: Postgraduate years 3 and 4 orthopedic residents in our program were asked to participate. The institutional review board reviewed and approved the study as exempt. RESULTS: Fracture repair constructs capable of resisting loads expected during rehabilitation were created by approximately half the residents tested. However, traditional written and computer-based testing methods failed to predict which resident's fracture construct would pass the biomechanical testing. Prior in vivo similar case experience was not predictive. CONCLUSIONS: The idea that "book smart does not equal street smart" applies to the tested model. To measure surgical skill acquisition and increase public safety related to surgery, it will be necessary to employ new and specific examination methods that identify the skill to be acquired and test the acquisition of this skill as precisely as possible.

Correlation of motor function and stereognosis impairment in upper limb cerebral palsy.

PURPOSE: To correlate motor function, as measured by the Jebsen-Taylor test, and sensory function, as measured by the 12-object stereognosis testing, in the hands of children with spastic hemiplegia due to cerebral palsy. METHODS: A chart review identified children with hemiplegic and triplegic cerebral palsy with stereognosis and Jebsen-Taylor testing between 1997 and 2008. Forty-one children were included in the study, including 22 girls and 19 boys, with an average age of 8.7 years (range, 6-16 years). The right side is affected in 23 children; 34 children have hemiplegic cerebral palsy, and 7 have triplegic cerebral palsy. The initial Jebsen-Taylor and stereognosis test results were recorded for each subject, as well as age, diagnosis, affected side, and prior treatment with hand therapy, botulinum toxin injection, or surgery. Descriptive statistics, chi-square analysis, paired t-tests, and correlation measurements were used for analysis of the data. RESULTS: Statistically significant inverse correlations exist between the cards, small objects, checkers, light objects, and heavy objects on the Jebsen-Taylor subtests, as correlated with the stereognosis scores in the affected hand (p < or = 0.04). The stereognosis scores for the patients who were not able to complete the Jebsen-Taylor test with the affected hand were significantly lower than those who were able to complete the Jebsen-Taylor test with the affected hand (p = .04). The stereognosis scores were significantly lower for the affected side as compared with the contralateral side. The Jebsen-Taylor total test times were significantly longer for the affected side as compared with the contralateral side (p < .001). CONCLUSIONS: In children with hemiplegic and triplegic cerebral palsy, the impairment of stereognosis is correlated with impairment in motor function, and the inability to complete the Jebsen-Taylor test with the affected hand is associated with impaired stereognosis function. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognostic IV.

Pulsed electromagnetic fields accelerate normal and diabetic wound healing by increasing endogenous FGF-2 release.

BACKGROUND: Chronic wounds, particularly in diabetics, result in significant morbidity and mortality and have a profound economic impact. The authors demonstrate that pulsed electromagnetic fields significantly improve both diabetic and normal wound healing in 66 mice through up-regulation of fibroblast growth factor (FGF)-2 and are able to prevent tissue necrosis in diabetic tissue after an ischemic insult. METHODS: Db/db and C57BL6 mice were wounded and exposed to pulsed electromagnetic fields. Gross closure, cell proliferation, and vascularity were assessed. Cultured medium from human umbilical vein endothelial cells exposed to pulsed electromagnetic fields was analyzed for FGF-2 and applied topically to wounds. Skin flaps were created on streptozocin-induced diabetic mice and exposed to pulsed electromagnetic fields. Percentage necrosis, oxygen tension, and vascularity were determined. RESULTS: Pulsed electromagnetic fields accelerated wound closure in diabetic and normal mice. Cell proliferation and CD31 density were significantly increased in pulsed electromagnetic field-treated groups. Cultured medium from human umbilical vein endothelial cells in pulsed electromagnetic fields exhibited a three-fold increase in FGF-2, which facilitated healing when applied to wounds. Skin on diabetic mice exposed to pulsed electromagnetic fields did not exhibit tissue necrosis and demonstrated oxygen tensions and vascularity comparable to those in normal animals. CONCLUSIONS: This study demonstrates that pulsed electromagnetic fields are able to accelerate wound healing under diabetic and normal conditions by up-regulation of FGF-2-mediated angiogenesis. They also prevented tissue necrosis in response to a standardized ischemic insult, suggesting that noninvasive angiogenic stimulation by pulsed electromagnetic fields may be useful to prevent ulcer formation, necrosis, and amputation in diabetic patients.

BRCA2 function in DNA binding and recombination from a BRCA2-DSS1-ssDNA structure.

Mutations in the BRCA2 (breast cancer susceptibility gene 2) tumor suppressor lead to chromosomal instability due to defects in the repair of double-strand DNA breaks (DSBs) by homologous recombination, but BRCA2's role in this process has been unclear. Here, we present the 3.1 angstrom crystal structure of a approximately 90-kilodalton BRCA2 domain bound to DSS1, which reveals three oligonucleotide-binding (OB) folds and a helix-turn-helix (HTH) motif. We also (i) demonstrate that this BRCA2 domain binds single-stranded DNA, (ii) present its 3.5 angstrom structure bound to oligo(dT)9, (iii) provide data that implicate the HTH motif in dsDNA binding, and (iv) show that BRCA2 stimulates RAD51-mediated recombination in vitro. These findings establish that BRCA2 functions directly in homologous recombination and provide a structural and biochemical basis for understanding the loss of recombination-mediated DSB repair in BRCA2-associated cancers.